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——睡眠能够抑制致使遗忘的神经细胞的活性

·未来|越睡越聪明

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(图片来自百度搜索)

小明,小明,快别睡了,起来背书  

妈妈,我这不是在睡觉,我这是为了记得更牢

 

下次睡懒觉被叫醒时,你可以光明正大的为自己的偷懒开脱罪名了。近期在《Cell》杂志上,美国Scripps研究所发表的最新研究成果表明:睡眠能够抑制致使遗忘的多巴胺能的活性从而来保护巩固记忆。

 

有关睡眠与记忆之间的关系,早期的神经科学家和心理学家已经进行了大量的研究。目前,比较流行的观点主要有两种,一种观点认为睡眠改善记忆的方式是通过阻断正在进行的干扰活动,如精神活动和外部的感觉刺激;另一种观点认为,睡眠能够加强突触的连接从而巩固记忆。

 

有的记忆可以持续很长时间,而更多的记忆随着时间消逝了。我们的大脑为什么会遗忘? 这个问题困扰了心理学家和神经科学家几个世纪了,甚至一度认为遗忘是大脑的一个缺陷。而这篇论文的通讯作者Ron Davis说:“科学家们都在试图阐明我们如何学习以及我们的记忆是如何巩固的,但是很少有人去研究遗忘的机制。”他说道,“遗忘是大脑的基本功能,它是对复杂多变的外部环境的一种生物适应。”

 

在此之前,科学家利用动物模型进行研究,揭示了特定的多巴胺神经元能够调控遗忘,但并没有阐明多巴胺能活性与睡眠之间的关系。Ron Davis等人利用果蝇模型的研究表明,多巴胺能的活性受行为状态的影响:利用药物或者光遗传刺激睡眠回路增加睡眠,能够减少多巴胺信号的活性,进而巩固记忆。这些发现支持了之前的神经科学家和心理学家的研究,从抑制遗忘的角度补充了睡眠改善巩固记忆的潜在机制。

 

 

 

下面附上与本文及与之相关的几篇文章摘要,以飨对这个领域感兴趣的小伙伴们。

 

 

1.      本文标题:标题为:Sleep FacilitatesMemory by Blocking Dopamine Neuron-Mediated Forgetting.

 

原文链接:点击打开链接


原文摘要:

Early studies from psychology suggest thatsleep facilitates memory retention by stopping ongoing retroactive interferencecaused by mental activity or external sensory stimuli. Neuroscience researchwith animal models, on the other hand, suggests that sleep facilitatesretention by enhancing memory consolidation. Recently, in Drosophila,the ongoing activity of specific dopamine neurons was shown to regulate theforgetting of olfactory memories. Here, we show this ongoing dopaminergicactivity is modulated with behavioral state, increasing robustly with locomotoractivity and decreasing with rest. Increasing sleep-drive, with either thesleep-promoting agent Gaboxadol or by genetic stimulation of the neuralcircuit for sleep, decreases ongoing dopaminergic activity, while enhancingmemory retention. Conversely, increasing arousal stimulates ongoingdopaminergic activity and accelerates dopaminergic-based forgetting. Therefore,forgetting is regulated by the behavioral state modulation ofdopaminergic-based plasticity. Our findings integrate psychological andneuroscience research on sleep and forgetting.

 

2.      论文标题:Dopamine IsRequired for Learning and Forgetting in Drosophila
原文摘要:Psychological studies inhumans and behavioral studies of model organisms suggest that forgetting is acommon and biologically regulated process, but the molecular, cellular, andcircuit mechanisms underlying forgetting are poorly understood. Here we show thatthe bidirectional modulation of a small subset of dopamine neurons (DANs) afterolfactory learning regulates the rate of forgetting of both punishing(aversive) and rewarding (appetitive) memories. Two of these DANs, MP1 and MV1,exhibit synchronized ongoing activity in the mushroom body neuropil in aliveand awake flies before and after learning, as revealed by functional cellularimaging. Furthermore, while the mushroom-body-expressed dDA1 dopamine receptoris essential for the acquisition of memory, we show that the dopamine receptorDAMB, also highly expressed in mushroom body neurons, is required forforgetting. We propose a dual role for dopamine: memory acquisition throughdDA1 signaling and forgetting through DAMB signaling in the mushroom body neurons.
全文链接:http://ac.els-cdn.com/S0896627312003388/1-s2.0-S0896627312003388-main.pdf?_tid=0c827be8-1598-11e5-aea8-00000aab0f01&acdnat=1434618029_63912fc12374978f0ad3994579ea046c

3.      论文标题:Forgetting IsRegulated through Rac Activity in Drosophila
原文摘要:Initially acquired memorydissipates rapidly if not consolidated. Such memory decay is thought to resulteither from the inherently labile nature of newly acquired memories or frominterference by subsequently attained information. Here we report that a smallG protein Rac-dependent forgetting mechanism contributes to both passive memorydecay and interference-induced forgetting in Drosophila. Inhibition of Racactivity leads to slower decay of early memory, extending it from a few hoursto more than one day, and to blockade of interference-induced forgetting.Conversely, elevated Rac activity in mushroom body neurons accelerates memorydecay. This forgetting mechanism does not affect memory acquisition and isindependent of Rutabaga adenylyl cyclase-mediated memory formation mechanisms.Endogenous Rac activation is evoked on different time scales during gradualmemory loss in passive decay and during acute memory removal in reversallearning. We suggest that Rac\'s role in actin cytoskeleton remodeling may contributeto memory erasure.
全文链接:http://ac.els-cdn.com/S0092867409016304/1-s2.0-S0092867409016304-main.pdf?_tid=d1d65b36-1597-11e5-8a2b-00000aab0f6c&acdnat=1434617931_2c24da5631cf681d9bf6bea68e8ea9f9

4.      论文标题:Dopaminergiccontrol of synaptic plasticity in the dorsal striatum
原文摘要:Cortical glutamatergic andnigral dopaminergic afferents impinge on projection spiny neurons of thestriatum, providing the most significant inputs to this structure. Isolatedactivation of glutamate or dopamine (DA) receptors produces short-term effectson striatal neurons, whereas the combined stimulation of both glutamate and DAreceptors is able to induce long-lasting modifications of synapticexcitability. Repetitive stimulation of corticostriatal fibres causes a massiverelease of both glutamate and DA in the striatum and, depending on theglutamate receptor subtype preferentially activated, produces either long-termdepression (LTD) or long-term potentiation (LTP) of excitatory synaptictransmission. D1-like and D2-like DA receptors interact synergistically toallow LTD formation, while they operate in opposition during the inductionphase of LTP. Corticostriatal synaptic plasticity is severely impaired afterchronic DA denervation and requires the stimulation of DARPP-32, a small proteinexpressed in dopaminoceptive spiny neurons which acts as a potent inhibitor ofprotein phosphatase-1. In addition, the formation of LTD and LTP requires theactivation of PKG and PKA, respectively, in striatal projection neurons. Thesekinases appear to be stimulated by the activation of D1-like receptors indistinct neuronal populations.
全文链接:http://onlinelibrary.wiley.com/doi/10.1046/j.0953-816x.2001.01485.x/pdf